[Glucocorticoid-induced reduction in NO bioavailability and vascular endothelial dysfunction].

Glucocorticoid excess enhances superoxide-induced inactivation of nitric oxide (NO) and suppresses NO production through decreasing the expression of endothelial NO synthase. Glucocorticoid-induced decrease in NO bioavailability elicits vasuclar endothelial dysfunction, leading to insufficiency of peripheral circulation, which may be the pathogenesis for idiopathic osteonecrosis of the femoral head (ION) . Glucocorticoid-induced vascular endothelial dysfunction is the major therapeutic target for ION. NO causes overproduction of reactive oxygen species.